Rheum Review

Question 1

What is one way to protect against OA?

Answer 1

Exercise

Question 2

What joint does OA hit that RA doesn’t?

Answer 2

DIP

Question 3

A drug inhibiting ________ would be a great treatment for OA.

Answer 3

Cytokine production

CONVERSELY. increasing MMP would be bad, because then it’s just eating more

Question 4

RA is a systemic, inflammatory, autoimmune disorder of unknown etiology that results predominantly in a peripheral ________ _______.

Answer 4

symmetric synovitis

Question 5

RA disease susceptibility and severity is associated with _________ in subtypes of _______ and _______

Answer 5

shared epitope (QKRAA; in antigen binding groove)
HLA-DR4 and HLA-DR1

Question 6

In RA, ____________ are pathogenic

Answer 6

RF-IgG immune complexes

Question 7

In RA, CD4+ memory T cells play an important role, namely:

Answer 7

modulation and amplification of local immune response through antigen recognition
(query altered proteoglycans or collagen; citrullinated peptides)

Question 8

Gout is the result of tissue deposition of monosodium urate (MSU) crystals due to hyperuricemia. Basically,

Answer 8

MSU supersaturation of extracellular fluids

Question 9

90% of the time, hyperuricemia is caused by __________.

Answer 9

UNDER EXCRETORS

Question 10

Uric acid is a product of _____ metabolism

Answer 10

Purine

Question 11

Humans lack _____ which oxidizes uric acid into allantoin.

Answer 11

uricase

Question 12

Two methods for a genetic disorder involving OVER production of uric acid:

Answer 12

PRPP synthetase overactivity
HGPRT deficiency (complete: Lesch-Nyhan)
both are X-linked

Question 13

Crystal arthritis is diagnosed by ______

Answer 13

arthrocentesis, uric acid level alone is not enough.

Question 14

MSU crystals appear as _____ and _____

Answer 14

NEEDLE-shaped, NEGATIVELY birefringent

Question 15

In gouty arthritis, Proteins coating the crystals modulate the cellular response, specifically by

Answer 15

IgG-coating promotes phagocytosis by PMNs
(IgG: not specific anti-crystal antibodies, more of a charge interaction)
Apolipoprotein B-coating INHIBITS phagocytosis

Question 16

CPPD crystals appear as

Answer 16

rhomboid, POSITIVELY birefringent

Question 17

In spondyloarthritis, the following joints are affected

Answer 17

SACROILIITIS (SI joint) and Spine

Question 18

Spondyloarthropathies specifically involve ________

Answer 18

Enthesitis: ligamentous-, tendinous-, fibrous-osseous junctions

Question 19

In spondyloarthropathies, the synovium shows _______

Answer 19

increased expression of TNFa

Question 20

Your chance of developing AS is __% if ______ positive, and jumps to __% if you also have ______.

Answer 20

2% if HLA-B27 positive

20% if you have a first-degree relative with AS, as well

Question 21

Reactive arthritis is asymmetric, oligoarticular (<5 joints), and mostly _________

Answer 21

lower ext arthritis

Question 22

SLE’s fundamental defect is the _____________, resulting in ___________. What cells are involved?

Answer 22

misdirected recognition of self as foreign
an autoimmune process
Both B and T cells

Question 23

In SLE, antibody responses toward autoantigens are ___________ and _____________.

Answer 23

antigen-driven and require CD4+ T cells

Question 24

In SLE, it’s a loss of __________ which permits _________, which is a _________ abnormality

Answer 24

Loss of T cell tolerance permitting autoreactive B cell stimulation; peripheral abnormality of self-reactive lymphocyte deletion or anergy

Question 25

What is the lupus gene?

Answer 25

Trick question, it’s POLYGENIC

Question 26

What is the greatest genetic association with SLE?

Answer 26

C4A null allele

Question 27

____% of lupus pts have a positive ANA, but the test is

Answer 27

95%, not specific for lupus

Question 28

A positive ANA shows Ab against _______

Answer 28

MULTIPLE nuclear antigens
Anti-dsDNA antibodies: renal disease
Anti-histone antibodies: SLE and drug-induced lupus
Antibodies to non-DNA, non-histone nuclear antigens:

Question 29

In SLE, anti-phospholipid Abs have an association with ______

Answer 29

increased clotting

Question 30

In SLE, you can also get what immunopathology?

Answer 30

Type III, IC complexes, resulting in glomerulonephritis (lumpy bumpy on IF)

Question 31

Describe how immune complexes result in vasculitis.

Answer 31

Immune complexes: inflamm→ PAFs→ ↑vascular permeability→ IC deposition; palpable purpura

Question 32

What is the relationship between T cells and endothelial injury?

Answer 32

HLA-DR4 and giant cell arteritis; suggests antigen-driven vascular inflammation

Question 33

cANCA involves ______ in primary granules of PMNs, associated with _________.
pANCA involves ______ in primary granules of PMNs, associated with _________.

Answer 33

Proteinase3; GPA (Wegner’s)

MPO; microscopic polyangiitis (MPA)

Question 34

What is the MAJOR manifestation (outside of muscles) of anti-synthetase syndrome?

Answer 34

ILD

Question 35

What are the anti-synthetase antibodies?

Answer 35

Anti-aminoacyl-tRNA synthetases (CYTOPLASM)
Anti-Jo-1 = anti-HISTADYL-tRNA synthetase
Not pathologic or myotoxic antibodies, they’re merely markers of disease

Question 36

On biopsy, polymyositis shows ___________ whereas dermatomyositis shows ___________.

Answer 36

CD8 T cells INSIDE muscle fibers (poly, think multiple, 8 > 4. So many, they can’t just hang outside)
CD4 T cells OUTSIDE muscle fibers

No live virus has been cultured from these